Since 1998, the Columbia Center for Children’s Environmental Health (CCCEH) has followed a New York City birth cohort to study the effects of prenatal and childhood exposures to polycyclic aromatic hydrocarbons (PAH) on neurodevelopmental outcomes through 12 years of age. Because of the heightened susceptibility of the developing fetus and young child, early exposures to PAH may be associated with excess risk for neurodevelopmental damage. Repeated waves of assessment in our cohort have revealed a picture of recurrent developmental abnormalities, including moderate cognitive delay at 3-5 years, and increased symptoms of anxiety/depression and attention problems at ages 6-9 years of age. Underlying these cognitive and behavioral anomalies, we have documented a persistent pattern of neurocognitive dysregulation, suggesting that highly exposed children fail to develop along the normal trajectory of improving self-regulatory control that accompanies maturity. We now propose to follow 350 cohort children through age 15-17 years, to assess the cognitive, emotional, and behavioral repercussions of PAH-associated dysregulation into the adolescent years--a critical developmental period in which conduct disturbances, social problems, substance use, and depressive symptoms frequently emerge for the first time, with serious adult consequences. We posit that prenatal PAH exposure will be associated with 1) neuropsychological deficits in reasoning, attentional, inhibitory and emotional control at 15-17 years ; 2) increased clinical symptoms (mood disturbances, high risk behaviors, and the persistence of ADHD symptoms); and 3) atypical developmental trajectories from early childhood through adolescence. This research is significant first because adolescent developmental disorders are serious and highly prevalent. Second, PAH exposures are widespread, yet their long-term effects are poorly understood due to limited exposure assessment. We address this limitation by using two complementary approaches to PAH exposure assessment: personal air monitoring and biomarkers of individual exposure/dose (PAH-DNA adducts). Third, this work rests on a strong brain-based theory that PAH exposure disrupts the developing organism’s capacity for self-regulatory control — a theory that unifies all 3 research projects in this application. The same children with PAH-associated self-regulatory problems (Project1) also manifest higher rates of obesity (Project 2). Neuroimaging in the same cohort suggests that prenatal PAH exposure leads to reduced white matter volumes and deficient self-regulation, providing preliminary yet compelling evidence that prenatal PAH effects on behavioral dysregulation are mediated by anatomical brain changes (Project 3). This study thus provides a unique opportunity to follow an existing cohort, with repeated measures of neuropsychological abilities from birth through the adolescent years, for the purpose of fully observing and better understanding the developmental impacts of PAH—one of the most widespread and toxic environmental contaminants. ExpandCollapse Abstract